: The conservation of the innate immune response signaling pathway in Drosophila, mice and humans has been well documented, and involves the recognition of pathogen-associated molecular patterns (PAMPs) by Toll-like receptors. A substantial body of both published work and preliminary results concerning signaling pathways that respond to the bacterial flagellar peptide, Flg22, or to oligogalacturonides (OGs) often released from plant cell walls upon pathogen infection has shown that both OGs and Flg22 behave as PAMPs and that their signaling pathways confer basal resistance to a wide spectrum of pathogens. Two general hypotheses that we propose to test are (1) that among the characterized plant immune response pathways, the OG and Flg22 pathways are among the most ancient and most similar to the so-called "Toll-like" innate immune signaling pathways characterized in Drosophila and mammals, and (2) that disease-causing pathogens have evolved virulence factors to target and block PAMP-elicited resistance. My goals are to identify Pseudomonas syringae type III effectors that disrupt or modify the OG signaling pathway to enhance pathogen virulence, and then to identify the OG signaling targets of these virulence effectors.